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Статті в журналах з теми "Legionella longbeachae"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 14 лютого 2022

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1

Chambers, Stephen T., Sandy Slow, Amy Scott-Thomas, and David R. Murdoch. "Legionellosis Caused by Non-Legionella pneumophila Species, with a Focus on Legionella longbeachae." Microorganisms 9, no. 2 (January 31, 2021): 291. http://dx.doi.org/10.3390/microorganisms9020291.

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Although known as causes of community-acquired pneumonia and Pontiac fever, the global burden of infection caused by Legionella species other than Legionella pneumophila is under-recognised. Non-L. pneumophila legionellae have a worldwide distribution, although common testing strategies for legionellosis favour detection of L. pneumophila over other Legionella species, leading to an inherent diagnostic bias and under-detection of cases. When systematically tested for in Australia and New Zealand, L. longbeachae was shown to be a leading cause of community-acquired pneumonia. Exposure to potting soils and compost is a particular risk for infection from L. longbeachae, and L. longbeachae may be better adapted to soil and composting plant material than other Legionella species. It is possible that the high rate of L. longbeachae reported in Australia and New Zealand is related to the composition of commercial potting soils which, unlike European products, contain pine bark and sawdust. Genetic studies have demonstrated that the Legionella genomes are highly plastic, with areas of the chromosome showing high levels of recombination as well as horizontal gene transfer both within and between species via plasmids. This, combined with various secretion systems and extensive effector repertoires that enable the bacterium to hijack host cell functions and resources, is instrumental in shaping its pathogenesis, survival and growth. Prevention of legionellosis is hampered by surveillance systems that are compromised by ascertainment bias, which limits commitment to an effective public health response. Current prevention strategies in Australia and New Zealand are directed at individual gardeners who use potting soils and compost. This consists of advice to avoid aerosols generated by the use of potting soils and use masks and gloves, but there is little evidence that this is effective. There is a need to better understand the epidemiology of L. longbeachae and other Legionella species in order to develop effective treatment and preventative strategies globally.

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2

Kozak, Natalia A., Meghan Buss, Claressa E. Lucas, Michael Frace, Dhwani Govil, Tatiana Travis, Melissa Olsen-Rasmussen, Robert F. Benson, and Barry S. Fields. "Virulence Factors Encoded by Legionella longbeachae Identified on the Basis of the Genome Sequence Analysis of Clinical Isolate D-4968." Journal of Bacteriology 192, no. 4 (December 11, 2009): 1030–44. http://dx.doi.org/10.1128/jb.01272-09.

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ABSTRACT Legionella longbeachae causes most cases of legionellosis in Australia and may be underreported worldwide due to the lack of L. longbeachae-specific diagnostic tests. L. longbeachae displays distinctive differences in intracellular trafficking, caspase 1 activation, and infection in mouse models compared to Legionella pneumophila, yet these two species have indistinguishable clinical presentations in humans. Unlike other legionellae, which inhabit freshwater systems, L. longbeachae is found predominantly in moist soil. In this study, we sequenced and annotated the genome of an L. longbeachae clinical isolate from Oregon, isolate D-4968, and compared it to the previously published genomes of L. pneumophila. The results revealed that the D-4968 genome is larger than the L. pneumophila genome and has a gene order that is different from that of the L. pneumophila genome. Genes encoding structural components of type II, type IV Lvh, and type IV Icm/Dot secretion systems are conserved. In contrast, only 42/140 homologs of genes encoding L. pneumophila Icm/Dot substrates have been found in the D-4968 genome. L. longbeachae encodes numerous proteins with eukaryotic motifs and eukaryote-like proteins unique to this species, including 16 ankyrin repeat-containing proteins and a novel U-box protein. We predict that these proteins are secreted by the L. longbeachae Icm/Dot secretion system. In contrast to the L. pneumophila genome, the L. longbeachae D-4968 genome does not contain flagellar biosynthesis genes, yet it contains a chemotaxis operon. The lack of a flagellum explains the failure of L. longbeachae to activate caspase 1 and trigger pyroptosis in murine macrophages. These unique features of L. longbeachae may reflect adaptation of this species to life in soil.

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3

Konecny, P., and A. J. Bell. "Positive Serology to Legionella Longbeachae in Patients with Adult Respiratory Distress Syndrome." Anaesthesia and Intensive Care 24, no. 6 (December 1996): 678–81. http://dx.doi.org/10.1177/0310057x9602400608.

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In an observational study we measured the Legionella longbeachae antibody titre rise in patients mechanically ventilated for more than eight days during a two-month period. The patients were divided into two groups on the basis of the presence or absence of the adult respiratory distress syndrome (ARDS). In nine patients with ARDS all showed an antibody rise consistent with recent infection with Legionella long-beachae with a rise in titre (six patients) or a high titre after eight to ten days of ventilation (three patients). Three patients without ARDS did not show a rise in titre. Culture of the environment, ventilator circuits, humidifiers and humidification water did not reveal an environmental source of Legionella longbeachae in the Intensive Care Unit. Legionella longbeachae may be implicated as a pathogenic organism in ARDS, or as a secondary nosocomial infection. Alternatively the antibody titre rise may represent an epiphenomenon and may not be related to Legionella longbeachae infection.

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4

Gea–Izquierdo, Enrique. "Legionella longbeachae y legionelosis." Journal of the Selva Andina Research Society 3, no. 1 (August 1, 2012): 66–67. http://dx.doi.org/10.36610/j.jsars.2012.030100066.

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5

Kümpers, Philipp, Andreas Tiede, Philip Kirschner, Jutta Girke, Arnold Ganser, and Dietrich Peest. "Legionnaires' disease in immunocompromised patients: a case report of Legionella longbeachae pneumonia and review of the literature." Journal of Medical Microbiology 57, no. 3 (March 1, 2008): 384–87. http://dx.doi.org/10.1099/jmm.0.47556-0.

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In addition to Legionella pneumophila, about 20 Legionella species have been documented as human pathogens. The majority of infections by non-pneumophila Legionella species occur in immunocompromised and splenectomized patients. Here, we report a case of ‘classical’ lobar pneumonia caused by Legionella longbeachae in a splenectomized patient receiving corticosteroids for chronic immune thrombocytopenia. Tests for Legionella antigen were negative. L. longbeachae was immediately detected in bronchoalveolar fluid by PCR and subsequently confirmed by culture on legionella-selective media. The features of Legionnaires' disease in immunocompromised patients with special emphasis on significance and detection of non-pneumophila species are reviewed.

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6

Gobin, Ivana, Milorad Susa, Gabrijela Begic, Elizabeth L. Hartland, and Miljenko Doric. "Experimental Legionella longbeachae infection in intratracheally inoculated mice." Journal of Medical Microbiology 58, no. 6 (June 1, 2009): 723–30. http://dx.doi.org/10.1099/jmm.0.007476-0.

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This study established an experimental model of replicative Legionella longbeachae infection in A/J mice. The animals were infected by intratracheal inoculation of 103–109 c.f.u. L. longbeachae serogroup 1 (USA clinical isolates D4968, D4969 and D4973). The inocula of 109, 108, 107 and 106 c.f.u. of all tested L. longbeachae serogroup 1 isolates were lethal for A/J mice. Inoculation of 105 c.f.u. L. longbeachae caused death in 90 % of the animals within 5 days, whilst inoculation of 104 c.f.u. caused sporadic death of mice. All animals that received 103 c.f.u. bacteria developed acute lower respiratory disease, but were able to clear Legionella from the lungs within 3 weeks. The kinetics of bacterial growth in the lungs was independent of inoculum size and reached a growth peak about 3 logarithms above the initial inoculum at 72 h after inoculation. The most prominent histological changes in the lungs were observed at 48–72 h after inoculation in the form of a focal, neutrophil-dominant, peribronchiolar infiltration. The inflammatory process did not progress towards the interstitial or alveolar spaces. Immunohistological analyses revealed L. longbeachae serogroup 1 during the early phase of infection near the bronchiolar epithelia and later co-localized with inflammatory cells. BALB/c and C57BL/6 mice strains were also susceptible to infection with all L. longbeachae serogroup 1 strains tested and very similar changes were observed in the lungs of infected animals. These results underline the infection potential of L. longbeachae serogroup 1, which is associated with high morbidity and lethality in mice.

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7

Saint, Christopher P., and Lionel Hot. "Legionella longbeachae isolated from water." Medical Journal of Australia 168, no. 2 (January 1998): 96. http://dx.doi.org/10.5694/j.1326-5377.1998.tb126736.x.

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8

Marais, Ophélie. "Une pneumonie à Legionella longbeachae." Option/Bio 21, no. 443 (October 2010): 5. http://dx.doi.org/10.1016/s0992-5945(10)70547-x.

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9

Montanaro-Punzengruber, J. C., L. Hicks, W. Meyer, and G. L. Gilbert. "Australian Isolates of Legionella longbeachae Are Not a Clonal Population." Journal of Clinical Microbiology 37, no. 10 (1999): 3249–54. http://dx.doi.org/10.1128/jcm.37.10.3249-3254.1999.

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Legionella longbeachae is almost as frequent a cause of legionellosis in Australia as Legionella pneumophila, but epidemiological investigation of possible environmental sources and clinical cases has been limited by the lack of a discriminatory subtyping method. The purpose of this study was to examine the genetic variability among Australian isolates of L. longbeachaeserogroup 1. Pulsed-field gel electrophoresis (PFGE) ofSfiI fragments revealed three distinct pulsotypes among 57 clinical and 11 environmental isolates and the ATCC control strains of L. longbeachae serogroups 1 and 2. Each pulsotype differed by four bands, corresponding to <65% similarity. A clonal subgroup within each pulsotype was characterized by >88% similarity. The largest major cluster was pulsotype A, which included 43 clinical isolates and 9 environmental isolates and was divided into five subgroups. Pulsotypes B and C comprised smaller numbers of clinical and environmental isolates, which could each be further divided into three subgroups. The ATCC type strain of L. longbeachae serogroup 1 was classified as pulsotype B, subtype B3, while the ATCC type strain of L. longbeachae serogroup 2 was identified as a different pulsotype, LL2. SfiI macrorestriction analysis followed by PFGE showed that the AustralianL. longbeachae strains are not a single clonal population as previously reported.

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10

OKAZAKI, Miki, Michio KOIDE, and Atsushi SAITO. "Legionella longbeachae Pneumonia in a Gardener." Journal of the Japanese Association for Infectious Diseases 72, no. 10 (1998): 1076–79. http://dx.doi.org/10.11150/kansenshogakuzasshi1970.72.1076.

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11

Sonesson, A., Erik Jantzen, Torill Tangen, and Ulrich Z�hringer. "Chemical composition of lipopolysaccharides from Legionella bozemanii and Legionella longbeachae." Archives of Microbiology 162, no. 4 (October 1, 1994): 215–21. http://dx.doi.org/10.1007/s002030050128.

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12

Sonesson, Anders, Erik Jantzen, Torill Tangen, and Ulrich Z�hringer. "Chemical composition of lipopolysaccharides from Legionella bozemanii and Legionella longbeachae." Archives of Microbiology 162, no. 4 (October 1994): 215–21. http://dx.doi.org/10.1007/bf00301841.

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13

Koide, Michio, Noriko Arakaki, and Atsushi Saito. "Distribution of Legionella longbeachae and other legionellae in Japanese potting soils." Journal of Infection and Chemotherapy 7, no. 4 (2001): 224–27. http://dx.doi.org/10.1007/s101560170017.

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14

Doyle, Robyn M., Nicholas P. Cianciotto, Shaila Banvi, Paul A. Manning, and Michael W. Heuzenroeder. "Comparison of Virulence ofLegionella longbeachae Strains in Guinea Pigs and U937 Macrophage-Like Cells." Infection and Immunity 69, no. 9 (September 1, 2001): 5335–44. http://dx.doi.org/10.1128/iai.69.9.5335-5344.2001.

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ABSTRACT A guinea pig model of experimental legionellosis was established for assessment of virulence of isolates of Legionella longbeachae. The results showed that there were distinct virulence groupings of L. longbeachae serogroup 1 strains based on the severity of disease produced in this model. Statistical analysis of the animal model data suggests that Australian isolates of L. longbeachae may be inherently more virulent than non-Australian strains. Infection studies performed with U937 cells were consistent with the animal model studies and showed that isolates of this species were capable of multiplying within these phagocytic cells. Electron microscopy studies of infected lung tissue were also undertaken to determine the intracellular nature of L. longbeachae serogroup 1 infection. The data showed that phagosomes containing virulent L. longbeachae serogroup 1 appeared bloated, contained cellular debris and had an apparent rim of ribosomes while those containing avirulent L. longbeachae serogroup 1 were compact, clear and smooth.

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15

Cloud, J. L., K. C. Carroll, P. Pixton, M. Erali, and D. R. Hillyard. "Detection of Legionella Species in Respiratory Specimens Using PCR with Sequencing Confirmation." Journal of Clinical Microbiology 38, no. 5 (2000): 1709–12. http://dx.doi.org/10.1128/jcm.38.5.1709-1712.2000.

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Legionella spp. are a common cause of community-acquired respiratory tract infections and an occasional cause of nosocomial pneumonia. A PCR method for the detection of legionellae in respiratory samples was evaluated and was compared to culture. The procedure can be performed in 6 to 8 h with a commercially available DNA extraction kit (Qiagen, Valencia, Calif.) and by PCR with gel detection. PCR is performed with primers previously determined to amplify a 386-bp product within the 16S rRNA gene of Legionella pneumophila. We can specifically detect the clinically significant Legionella species including L. pneumophila, L. micdadei, L. longbeachae, L. bozemanii, L. feeleii, and L. dumoffii. The assay detects 10 fg (approximately two organisms) of legionella DNA in each PCR. Of 212 clinical specimens examined by culture, 100% of the culture-positive samples (31 of 31) were positive by this assay. By gel detection of amplification products, 12 of 181 culture-negative samples were positive forLegionella species by PCR, resulting in 93% specificity. Four of the 12 samples with discrepant results (culture negative, PCR positive) were confirmed to be positive for Legionellaspecies by sequencing of the amplicons. The legionella-specific PCR assay that is described demonstrates high sensitivity and high specificity for routine detection of legionellae in respiratory samples.

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16

Asare, Rexford, Marina Santic, Ivana Gobin, Miljenko Doric, Jill Suttles, James E. Graham, Christopher D. Price, and Yousef Abu Kwaik. "Genetic Susceptibility and Caspase Activation in Mouse and Human Macrophages Are Distinct for Legionella longbeachae and L. pneumophila." Infection and Immunity 75, no. 4 (January 29, 2007): 1933–45. http://dx.doi.org/10.1128/iai.00025-07.

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ABSTRACT Legionella pneumophila is the predominant cause of Legionnaires' disease in the United States and Europe, while Legionella longbeachae is the common cause of the disease in Western Australia. Although clinical manifestations by both intracellular pathogens are very similar, recent studies have shown that phagosome biogeneses of both species within human macrophages are distinct (R. Asare and Y. Abu Kwaik, Cell. Microbiol., in press). Most inbred mouse strains are resistant to infection by L. pneumophila, with the exception of the A/J mouse strain, and this genetic susceptibility is associated with polymorphism in the naip5 allele and flagellin-mediated early activation of caspase 1 and pyropoptosis in nonpermissive mouse macrophages. Here, we show that genetic susceptibility of mice to infection by L. longbeachae is independent of allelic polymorphism of naip5. L. longbeachae replicates within bone marrow-derived macrophages and in the lungs of A/J, C57BL/6, and BALB/c mice, while L. pneumophila replicates in macrophages in vitro and in the lungs of the A/J mouse strain only. Quantitative real-time PCR studies on infected A/J and C57BL/6 mouse bone marrow-derived macrophages show that both L. longbeachae and L. pneumophila trigger similar levels of naip5 expression, but the levels are higher in infected C57BL/6 mouse macrophages. In contrast to L. pneumophila, L. longbeachae has no detectable pore-forming activity and does not activate caspase 1 in A/J and C57BL/6 mouse or human macrophages, despite flagellation. Unlike L. pneumophila, L. longbeachae triggers only a modest activation of caspase 3 and low levels of apoptosis in human and murine macrophages in vitro and in the lungs of infected mice at late stages of infection. We conclude that despite flagellation, infection by L. longbeachae is independent of polymorphism in the naip5 allele and L. longbeachae does not trigger the activation of caspase 1, caspase 3, or late-stage apoptosis in mouse and human macrophages. Neither species triggers caspase 1 activation in human macrophages.

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17

Lim, Irene, Norma Sangster, Janice A. Lanser, and Donald P. Reid. "Legionella longbeachae pneumonia: report of two cases." Medical Journal of Australia 150, no. 10 (May 1989): 599–601. http://dx.doi.org/10.5694/j.1326-5377.1989.tb136700.x.

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18

Steele, Trevor W. "The ecology of Legionella longbeachae in Australia." Medical Journal of Australia 164, no. 11 (June 1996): 703–4. http://dx.doi.org/10.5694/j.1326-5377.1996.tb122259.x.

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19

Crawford, Geoffrey R. "The ecology of Legionella longbeachae in Australia." Medical Journal of Australia 164, no. 11 (June 1996): 703–4. http://dx.doi.org/10.5694/j.1326-5377.1996.tb122260.x.

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20

Isenman, Heather, Trevor Anderson, Stephen T. Chambers, Roslyn G. Podmore, and David R. Murdoch. "Antimicrobial susceptibilities of clinical Legionella longbeachae isolates." Journal of Antimicrobial Chemotherapy 73, no. 4 (December 19, 2017): 1102–4. http://dx.doi.org/10.1093/jac/dkx484.

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21

Speers, David J., and Anthony E. Tribe. "Legionella longbeachae pneumonia associated with potting mix." Medical Journal of Australia 161, no. 8 (October 1994): 509. http://dx.doi.org/10.5694/j.1326-5377.1994.tb127576.x.

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22

GOWARDMAN, J. R., and J. HAVILL. "Legionella longbeachae pneumonia and Henoch-Schönlein purpura." Australian and New Zealand Journal of Medicine 26, no. 2 (April 1996): 236–37. http://dx.doi.org/10.1111/j.1445-5994.1996.tb00895.x.

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23

Doyle, Robyn M., Trevor W. Steele, Alan M. McLennan, Ian H. Parkinson, Paul A. Manning, and Michael W. Heuzenroeder. "Sequence Analysis of the mip Gene of the Soilborne Pathogen Legionella longbeachae." Infection and Immunity 66, no. 4 (April 1, 1998): 1492–99. http://dx.doi.org/10.1128/iai.66.4.1492-1499.1998.

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ABSTRACT To understand the basis of pathogenesis by Legionella longbeachae serogroup 1, the importance of the Mip protein in this species was examined. Amino-terminal analysis of the purified, cloned L. longbeachae serogroup 1 ATCC 33462 Mip protein confirmed that the cloned gene protein was expressed and processed in an Escherichia coli background. DNA sequence analysis of plasmid pIMVS27, containing the entire L. longbeachaeserogroup 1 mip gene, revealed a high degree of homology to the mip gene of Legionella pneumophilaserogroup 1, 76% homology at the DNA level and 87% identity at the amino acid level. Primer extension analysis determined that the start site of transcription was the same for both species, with some differences observed for the −10 and −35 promoter regions. Primers designed from the mip gene sequence obtained forL. longbeachae serogroup 1 ATCC 33462 were used to amplify the mip genes from L. longbeachaeserogroup 2 ATCC 33484 and an Australian clinical isolate of L. longbeachae serogroup 1 A5H5. The mip gene from A5H5 was 100% identical to the type strain sequence. The serogroup 2 strain of L. longbeachae differed by 2 base pairs in third-codon positions. Allelic exchange mutagenesis was used to generate an isogenic mip mutant in ATCC 33462 and strain A5H5. The ATCCmip mutant was unable to infect a strain ofAcanthamoebae sp. both in liquid and in a potting mix coculture system, while the A5H5 mip mutant behaved in a manner siilar to that of L. pneumophilaserogroup 1, i.e., it displayed a reduced capacity to infect and multiply within Acanthamoebae. To determine if this mutation resulted in reduced virulence in the guinea pig animal model, the A5H5 mip mutant and its parent strain were assessed for their abilities to establish an infection after aerosol exposure. Unlike the virulent parent strain, the mutant strain did not kill any animals under two different dose regimes. The data indicate that the Mip protein plays an important role in the intracellular life cycle ofL. longbeachae serogroup 1 species and is required for full virulence.

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24

Desgranges, Florian, Alix T. Coste, Diane Wernly, Justine Dufour, Onya Opota, and Sylvain Meylan. "Immunosuppressed gardener pricked by roses grows Legionella longbeachae." Lancet 395, no. 10224 (February 2020): 604. http://dx.doi.org/10.1016/s0140-6736(20)30112-4.

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25

YAMAMOTO, Keizo, Yasunobu NODA, Hideo GONDA, Takashi OISHI, Yoshimasa TANIKAWA, and Eiko YABUUCHI. "A Survival Case of Severe Legionella longbeachae Pneumonia." Journal of the Japanese Association for Infectious Diseases 75, no. 3 (2001): 213–18. http://dx.doi.org/10.11150/kansenshogakuzasshi1970.75.213.

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26

Aoki, S., Y. Hirakata, Y. Miyazaki, K. Izumikawa, K. Yanagihara, K. Tomono, Y. Yamada, T. Tashiro, S. Kohno, and S. Kamihira. "Detection of Legionella DNA by PCR of whole-blood samples in a mouse model." Journal of Medical Microbiology 52, no. 4 (April 1, 2003): 325–29. http://dx.doi.org/10.1099/jmm.0.04999-0.

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A detection system for Legionella DNA in blood samples based on the PCR was developed and evaluated in A/J mice with experimentally induced Legionella pneumonia. Primers were designed to amplify a 106 bp DNA fragment of the 16S rRNA gene specific to Legionella species. The PCR system could detect clinically relevant Legionella species including Legionella pneumophila, Legionella micdadei, Legionella bozemanae, Legionella dumoffii, Legionella longbeachae, Legionella gormanii and Legionella jordanis. The sensitivity of the PCR system was 20 fg extracted DNA. In the mouse model, the blood PCR was compared with results obtained by PCR on bronchoalveolar lavage fluid (BALF) samples, cultures of blood and BALF and detection of Legionella urinary antigen. Blood PCR was positive until 8 days after infection, while BALF PCR became negative on day 4. These results indicate that PCR using blood samples may be a useful, convenient and non-invasive method for the diagnosis of Legionella pneumonia.

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27

Nimmo, Graeme R., and Jennifer Z. Bull. "Comparative susceptibility of Legionella pneumophila and Legionella longbeachae to 12 antimicrobial agents." Journal of Antimicrobial Chemotherapy 36, no. 1 (1995): 219–23. http://dx.doi.org/10.1093/jac/36.1.219.

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28

Boyle, S., G. Olive, N. Townell, A. Henderson, S. Bowler, and S. Blum. "Legionella longbeachae pneumonia as a complication of alemtuzumab therapy." Journal of Clinical Neuroscience 46 (December 2017): 67–69. http://dx.doi.org/10.1016/j.jocn.2017.08.051.

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29

Steele, T. W., J. Lanser, and N. Sangster. "Isolation of Legionella longbeachae serogroup 1 from potting mixes." Applied and Environmental Microbiology 56, no. 1 (1990): 49–53. http://dx.doi.org/10.1128/aem.56.1.49-53.1990.

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30

Dhillon, Rohan, Tarun Bastiampillai, and Sharon Hong. "An Unusual Case of Hospital-Acquired Infection: Legionella Longbeachae." Australasian Psychiatry 17, no. 4 (January 1, 2009): 337–38. http://dx.doi.org/10.1080/10398560802673022.

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31

Lindsay, D. S. J., A. W. Brown, D. J. Brown, S. J. Pravinkumar, E. Anderson, and G. F. S. Edwards. "Legionella longbeachae serogroup 1 infections linked to potting compost." Journal of Medical Microbiology 61, no. 2 (February 1, 2012): 218–22. http://dx.doi.org/10.1099/jmm.0.035857-0.

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32

Steele, T. W., C. V. Moore, and N. Sangster. "Distribution of Legionella longbeachae serogroup 1 and other legionellae in potting soils in Australia." Applied and Environmental Microbiology 56, no. 10 (1990): 2984–88. http://dx.doi.org/10.1128/aem.56.10.2984-2988.1990.

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33

Gabbay, Eli, W. Bastion De Boer, Justin A. Waring, and Quentin A. Summers. "Legionella longbeachae in Western Australia: a 12‐month retrospective review." Medical Journal of Australia 164, no. 11 (June 1996): 704. http://dx.doi.org/10.5694/j.1326-5377.1996.tb122261.x.

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34

T. Chambers, Stephen, Sandy Slow, Alice Withers, Michael Chim, Krista Dawson, John Clemens, Trevor Anderson, Jonathan Williman, David Murdoch, and Amy Scott-Thomas. "Pine Species Provide a Niche for Legionella Longbeachae." Journal of Applied & Environmental Microbiology 8, no. 2 (November 2, 2020): 46–52. http://dx.doi.org/10.12691/jaem-8-2-2.

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35

García-Somoza, María Dolores, Anabel Fernández, Enric Prats, and Ricardo Verdaguer. "Neumonía comunitaria por Legionella longbeachae serogrupo 1 en paciente inmunocompetente." Enfermedades Infecciosas y Microbiología Clínica 28, no. 6 (June 2010): 398–99. http://dx.doi.org/10.1016/j.eimc.2009.07.006.

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36

Wei, Sung-Hsi, Lei-Ron Tseng, Jei-Kai Tan, Chin-Yu Cheng, Yen-Tao Hsu, En-Tsung Cheng, Chia-Sheng Lu, et al. "Legionnaires’ disease caused by Legionella longbeachae in Taiwan, 2006–2010." International Journal of Infectious Diseases 19 (February 2014): 95–97. http://dx.doi.org/10.1016/j.ijid.2013.10.004.

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37

Steele, T. W., and A. M. McLennan. "Infection of Tetrahymena pyriformis by Legionella longbeachae and other Legionella species found in potting mixes." Applied and environmental microbiology 62, no. 3 (1996): 1081–83. http://dx.doi.org/10.1128/aem.62.3.1081-1083.1996.

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38

Feldman, Michal, and Gil Segal. "A Specific Genomic Location within the icm/dot Pathogenesis Region of Different Legionella Species Encodes Functionally Similar but Nonhomologous Virulence Proteins." Infection and Immunity 72, no. 8 (August 2004): 4503–11. http://dx.doi.org/10.1128/iai.72.8.4503-4511.2004.

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ABSTRACT Legionella pneumophila, the major causative agent of Legionnaires' disease, is a facultative intracellular pathogen that grows within human macrophages and amoebae. Intracellular growth involves the formation of a replicative phagosome that requires the Icm/Dot type IV secretion system. Part of the icm/dot region in L. pneumophila contains the icmTSRQPO genes. The proteins encoded by the icmR and icmQ genes were shown to exhibit a chaperone-substrate relationship. Analysis of this region from other pathogenic Legionella species, i.e., L. micdadei and L. longbeachae, indicated that the overall organization of this region is highly conserved, but it was found to contain a favorable site for gene variation. In the place where the icmR gene was expected to be located, other open reading frames that are nonhomologous to each other or to any entry in the GenBank database were found (migAB in L. micdadei and ligB in L. longbeachae). Examination of these unique genes revealed an outstanding phenomenon; by use of interspecies complementation, the icmR, migB, and ligB gene products were found to be functionally similar. In addition, the function of these proteins was usually dependent on the presence of the corresponding IcmQ proteins. Moreover, each of these proteins (IcmR, LigB, and MigB) was found to interact with the corresponding IcmQ proteins, and the genes encoding these proteins were found to be regulated by CpxR. This study reveals new evidence of gene variation occurring in the same genomic location within the icm/dot locus in various Legionella species. The genes found at this site were shown to be similarly regulated and to encode species-specific, nonhomologous, but functionally similar proteins.

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39

Derriennic, M., D. Villers, A. E. Reynaud, A. L. Courtieu, and F. Nicolas. "Infection pulmonaire a Legionella longbeachae serogroupe 1 chez un patient immunodeprime." Médecine et Maladies Infectieuses 17, no. 12 (December 1987): 736–37. http://dx.doi.org/10.1016/s0399-077x(87)80179-8.

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40

Grove, D. I., P. J. Lawson, J. S. Burgess, J. L. Moran, M. S. O'Fathartaigh, and W. E. Winslow. "An outbreak of Legionella longbeachae infection in an intensive care unit?" Journal of Hospital Infection 52, no. 4 (December 2002): 250–58. http://dx.doi.org/10.1053/jhin.2002.1322.

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41

Diederen, B. M. W., A. A. Zwet, A. Zee, and M. F. Peeters. "Community-acquired pneumonia caused by Legionella longbeachae in an immunocompetent patient." European Journal of Clinical Microbiology & Infectious Diseases 24, no. 8 (August 2005): 545–48. http://dx.doi.org/10.1007/s10096-005-1368-9.

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42

Lang, Ruth, Z. Wiler, J. Manor, R. Kazak, and Ida Boldur. "Legionella longbeachae pneumonia in a patient splenectomized for hairy-cell leukemia." Infection 18, no. 1 (January 1990): 31–32. http://dx.doi.org/10.1007/bf01644179.

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43

Neumeister, B., G. Reiff, M. Faigle, K. Dietz, H. Northoff, and F. Lang. "Influence of Acanthamoeba castellanii on Intracellular Growth of Different Legionella Species in Human Monocytes." Applied and Environmental Microbiology 66, no. 3 (March 1, 2000): 914–19. http://dx.doi.org/10.1128/aem.66.3.914-919.2000.

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ABSTRACT Previous studies using a murine model of coinhalation ofLegionella pneumophila and Hartmannella vermiformis have shown a significantly enhanced intrapulmonary growth of L. pneumophila in comparison to inhalation of legionellae alone (J. Brieland, M. McClain, L. Heath, C. Chrisp, G. Huffnagle, M. LeGendre, M. Hurley, J. Fantone, and C. Engleberg, Infect. Immun. 64:2449–2456, 1996). In this study, we introduce an in vitro coculture model of legionellae, Mono Mac 6 cells (MM6) andAcanthamoeba castellanii, using a cell culture chamber system which separates both cell types by a microporous polycarbonate membrane impervious to bacteria, amoebae, and human cells. WhereasL. pneumophila has shown a maximal 4-log-unit multiplication within MM6, which could not be further increased by coculture with Acanthamoeba castellanii, significantly enhanced replication of L. gormanii, L. micdadei, L. steigerwaltii, L. longbeachae, and L. dumoffii was seen after coculture with amoebae. This effect was seen only with uninfected amoebae, not with Legionella-infected amoebae. The supporting effect for intracellular multiplication in MM6 could be reproduced in part by addition of a cell-free coculture supernatant obtained from a coincubation experiment with uninfected A. castellanii andLegionella-infected MM6, suggesting that amoeba-derived effector molecules are involved in this phenomenon. This coculture model allows investigations of molecular and biochemical mechanisms which are responsible for the enhancement of intracellular multiplication of legionellae in monocytic cells after interaction with amoebae.

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44

O'CONNOR, B. A., J. CARMAN, K. ECKERT, G. TUCKER, R. GIVNEY, and S. CAMERON. "Does using potting mix make you sick? Results from a Legionella longbeachae case-control study in South Australia." Epidemiology and Infection 135, no. 1 (June 19, 2006): 34–39. http://dx.doi.org/10.1017/s095026880600656x.

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A case-control study was performed in South Australia to determine if L. longbeachae infection was associated with recent handling of commercial potting mix and to examine possible modes of transmission. Twenty-five laboratory-confirmed cases and 75 matched controls were enrolled between April 1997 and March 1999. Information on underlying illness, smoking, gardening exposures and behaviours was obtained by telephone interviews. Recent use of potting mix was associated with illness (OR 4·74, 95% CI 1·65–13·55, P=0·004) in bivariate analysis only. Better predictors of illness in multivariate analysis included poor hand-washing practices after gardening, long-term smoking and being near dripping hanging flower pots. Awareness of a possible health risk with potting mix protected against illness. Results are consistent with inhalation and ingestion as possible modes of transmission. Exposure to aerosolized organisms and poor gardening hygiene may be important predisposing factors to L. longbeachae infection.

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45

Wang, Jin-Yong, Xing Li, Jian-Yong Chen, and Bo Tong. "Epileptic Seizure after Use of Moxifloxacin in Man with Legionella longbeachae Pneumonia." Emerging Infectious Diseases 26, no. 11 (November 2020): 2725–27. http://dx.doi.org/10.3201/eid2611.191815.

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46

Eitrem, Rickard, Arne Forsgren, and Christer Nilsson. "Pneumonia and Acute Pancreatitis Most Probably Caused by a Legionella longbeachae Infection." Scandinavian Journal of Infectious Diseases 19, no. 3 (January 1987): 381–82. http://dx.doi.org/10.3109/00365548709018486.

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47

Cameron, R. L., K. G. J. Pollock, D. S. J. Lindsay, and E. Anderson. "Comparison of Legionella longbeachae and Legionella pneumophila cases in Scotland; implications for diagnosis, treatment and public health response." Journal of Medical Microbiology 65, no. 2 (February 1, 2016): 142–46. http://dx.doi.org/10.1099/jmm.0.000215.

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48

Gobin, I., M. Sarec, K. Selenic, M. Doric, and M. Susa. "P1742 Rapid systemic propagation of Legionella longbeachae lung infection in A/J mice." International Journal of Antimicrobial Agents 29 (March 2007): S494—S495. http://dx.doi.org/10.1016/s0924-8579(07)71581-9.

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49

Lanser, J. A., M. Adams, R. Doyle, N. Sangster, and T. W. Steele. "Genetic relatedness of Legionella longbeachae isolates from human and environmental sources in Australia." Applied and Environmental Microbiology 56, no. 9 (1990): 2784–90. http://dx.doi.org/10.1128/aem.56.9.2784-2790.1990.

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50

Amodeo, M. R., D. R. Murdoch, and A. D. Pithie. "Legionnaires’ disease caused by Legionella longbeachae and Legionella pneumophila: comparison of clinical features, host-related risk factors, and outcomes." Clinical Microbiology and Infection 16, no. 9 (September 2010): 1405–7. http://dx.doi.org/10.1111/j.1469-0691.2009.03125.x.

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